Granulocyte colony-stimulating factor may promote proliferation of human bladder cancer cells mediated by basic fibroblast growth factor.

Abstract

To investigate whether granulocyte colony-stimulating factor (G-CSF) promotes the proliferation of two bladder cancer cell lines, and to assess the mechanism of tumor proliferation in terms of cytokine expression. The proliferation of two bladder cancer cell lines derived from transitional cell carcinoma (KK-47 and T-24) was assessed by using the double-layer soft agarose colony assay in combination with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Seven cytokines were measured in the culture supernatant. Expression of granulocyte colony-stimulating factor (G-CSF) receptor and fibroblast growth factor (FGF) receptor mRNA was studied by means of reverse transcriptase polymerase chain reaction (RT-PCR). Recombinant human G-CSF (rhG-CSF) caused greater induction of the proliferation of KK-47 cells in the presence than in the absence of peripheral blood mononuclear cells (PBMCs) and its effect was dose-dependent. In contrast, rhG-CSF did not stimulate the proliferation of T-24 cells. Among several cytokines measured, only basic FGF was elevated in cultures of KK-47 cells with or without PBMCs. The basic FGF level was significantly increased by rhG-CSF stimulation in a dose-dependent manner. Specific PCR products for the G-CSF and FGF receptors were observed in KK-47 cells as well as PBMC, while no G-CSF receptor was detected in T-24 cells. rhG-CSF may promote the proliferation of KK-47 cells, probably via an increase in basic FGF production.